Genes (41)
Species: human : 40 mouse : 1 | |
Mouse | CD38 | 952 | CD38 molecule | The murine BP-3 gene encodes a relative of the CD38/NAD glycohydrolase family. Analysis of the BP-3 cDNA sequence indicates that it represents a previously undescribed gene that shares significant homology with genes encoding nicotinamide adenine dinucleotide (NAD) glycohydrolase of Aplysia californica and the CD38 antigens in mouse and human. | Human | CMM4 | 474388 | Melanoma, cutaneous malignant, 4 | Atypical nevi often present in non-sun exposed areas Atypical nevi (>5mm with irregular edge and pigmentation) | Human | MIA3 | 375056 | melanoma inhibitory activity family, member 3 | A small reduction of TANGO was also seen in different benign and atypical nevi when compared to normal skin. | Human | AKR1B10 | 57016 | aldo-keto reductase family 1, member B10 (aldose reductase) | Diabetes-induced alterations in the sorbitol pathway occur in sympathetic ganglia and therapeutic agents which inhibit aldose reductase or sorbitol dehydrogenase improve or exacerbate, respectively, diabetes-induced NAD. | Human | BBC3 | 27113 | BCL2 binding component 3 | Here we report that PUMA expression is significantly weaker in primary melanomas compared to dysplastic nevi (P_lt_0.0001), and is further reduced in metastatic melanomas compared to primary tumors (P=0.001). We used tissue microarray and immunohistochemistry to examine PUMA expression in 107 primary melanomas, 51 metastatic melanomas, and 64 dysplastic nevi. | Human | COPS5 | 10987 | COP9 signalosome subunit 5 | Jab1 was expressed in 14 (82%) standard nevi, 18 (95%) dysplastic nevi, 17 (77%) melanomas, and 16 (53%) of the metastatic melanomas (P<0.01). | Human | NAMPT | 10135 | nicotinamide phosphoribosyltransferase | Pre-B-cell colony-enhancing factor, whose expression is up-regulated in activated lymphocytes, is a nicotinamide phosphoribosyltransferase, a cytosolic enzyme involved in NAD biosynthesis. | Human | PLA2G6 | 8398 | phospholipase A2, group VI (cytosolic, calcium-independent) | Furthermore, the activation of PLA2 induced by the H-toxin was enhanced in the presence of NAD. | Human | VCAM1 | 7412 | vascular cell adhesion molecule 1 | METHODS. Sections of 20 nevocellular nevi, 35 dysplastic nevi, 6 melanomas in situ, and 20 malignant melanomas were investigated with respect to their expression of intercellular adhesion molecule-1 (ICAM-1), inducible cell adhesion molecule-110 (INCAM-110)/vascular cell adhesion molecule-1 (VCAM-1), E-selectin, lymphocyte function-associated antigen-1 (LFA-1), and the integrins for very late antigen-(VLA) alpha-(alpha) 2 and VLA-alpha 6; for these studies, monoclonal antibodies were used and indirect immunoperoxidase and immunofluorescence staining methods were performed. | Human | TXN | 7295 | thioredoxin | These mutants included ubi, nad, cys, nar, trx, grx, gsh and sod. | Human | TRH | 7200 | thyrotropin-releasing hormone | The presence of TRH in dysplastic nevi may be predictive for the development of melanoma | Human | TP53 | 7157 | tumor protein p53 | p53 alterations commence as early as at the stage of benign and dysplastic nevi but there is no concordance between the frequent p53 protein expression and the rarity of both TP53 gene mutations in melanomas | Human | STAT3 | 6774 | signal transducer and activator of transcription 3 (acute-phase response factor) | The findings presented here suggest that down-regulation of the transcription factors Stat1 and Stat3 by systemic IFN-alpha treatment may represent a potential pathway to prevent the activation of gene(s) whose expression may be required for atypical nevus cells to progress to melanoma. To explore clinical treatments that might interfere with and possibly prevent atypical nevus progression, a previous study documented that 3 months systemic low-dose interferon-alpha (IFN-alpha) treatment of patients with a clinical history of melanoma and numerous atypical nevi, led to inactivation of the STAT1 and STAT3 transcription factors in atypical nevi. Based upon this finding, we initiated a second study to determine whether systemic low-dose IFN-alpha treatment also impairs the expression of upstream regulators and downstream targets of STAT1 and STAT3 in atypical nevi. MATERIALS AND METHODS: To determine whether IFN-alpha, used for adjuvant therapy of high-risk, resected melanoma, induces changes in Stat3 in atypical nevi, patients with a clinical history of melanoma who have multiple atypical nevi were treated for 3 months with low-dose IFN-alpha. | Human | STAT1 | 6772 | signal transducer and activator of transcription 1, 91kDa | Based upon this finding, we initiated a second study to determine whether systemic low-dose IFN-alpha treatment also impairs the expression of upstream regulators and downstream targets of STAT1 and STAT3 in atypical nevi. The findings presented here suggest that down-regulation of the transcription factors Stat1 and Stat3 by systemic IFN-alpha treatment may represent a potential pathway to prevent the activation of gene(s) whose expression may be required for atypical nevus cells to progress to melanoma. To explore clinical treatments that might interfere with and possibly prevent atypical nevus progression, a previous study documented that 3 months systemic low-dose interferon-alpha (IFN-alpha) treatment of patients with a clinical history of melanoma and numerous atypical nevi, led to inactivation of the STAT1 and STAT3 transcription factors in atypical nevi. | Human | SSX2 | 6757 | synovial sarcoma, X breakpoint 2 | Thirty-four of 101 primary and metastatic melanoma cases and 2 of 24 common nevocellular and atypical nevus cases showed SSX nuclear staining. | Human | SPARC | 6678 | secreted protein, acidic, cysteine-rich (osteonectin) | Immunohistochemical analysis showed that SPARC was strongly expressed in 100% of primary melanomas (7 of 7) and metastatic melanomas (29 of 29), moderately expressed in most of the positive dysplastic nevi (13 of 14), and only weakly expressed in nevocellular nevi (4 of 25). | Human | SLC2A2 | 6514 | solute carrier family 2 (facilitated glucose transporter), member 2 | We examined them morphologically and measured islet NAD + NADH content, streptozotocin metabolite accumulation, glucose transport capacity, Glut2 levels and medium nitrite accumulation. | Human | PRPH | 5630 | peripherin | We evaluated by immunohistochemistry 74 cutaneous melanocytic lesions including primary invasive malignant melanoma (IMM), melanoma in situ (MIS), atypical nevus (nevus with architectural disorder and cytologic atypia of melanocytes) (AN), spindle and epithelioid cell nevus (Spitz nevus) (SN), blue nevus (BN), and common intradermal benign melanocytic nevus (BMN) for expression of peripherin. | Human | NME1 | 4830 | NME/NM23 nucleoside diphosphate kinase 1 | OBJECTIVE: We have analyzed expression of nm23 polypeptide in acquired melanocytic nevi (n = 19), dysplastic nevi (n = 19), malignant melanomas (n = 22) and metastases of malignant melanomas (n = 47) in situ. | Human | MSH2 | 4436 | mutS homolog 2, colon cancer, nonpolyposis type 1 (E. coli) | positive staining was found in 33.3% and 53.3% for hMLH1 and hMSH2, respectively, in dysplastic nevi, and in 54.5% and 69.1%, respectively, in cutaneous melanoma | Human | MMP15 | 4324 | matrix metallopeptidase 15 (membrane-inserted) | Expression of MT1-MMP, MT2-MMP, MT3-MMP and MMP-2 in nevocellular nevus (n = 5), dysplastic nevus (n = 2) and juvenile melanoma (n = 3) was undetectable or detected in only a few cells. | Human | MLH1 | 4292 | mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli) | positive staining was found in 33.3% and 53.3% for hMLH1 and hMSH2, respectively, in dysplastic nevi, and in 54.5% and 69.1%, respectively, in cutaneous melanoma | Human | MCM2 | 4171 | minichromosome maintenance complex component 2 | MCM protein 2 is present in melanocytes from benign nevi, dysplastic nevi, primary cutaneous melanomas, and cutaneous melanoma metastases | Human | MC1R | 4157 | melanocortin 1 receptor (alpha melanocyte stimulating hormone receptor) | Atypical nevi often present in non-sun exposed areas Atypical nevi (>5mm with irregular edge and pigmentation) | Human | LSP1 | 4046 | lymphocyte-specific protein 1 | We now show that overexpression of LSP1 produces F-actin bundles that are likely responsible for the morphologic and motile abnormalities characteristic of the NAD 47/89 phenotype. Therefore, these studies show that overexpression of LSP1 alone can recreate the morphologic and motile defects seen in NAD 47/89 and suggest that LSP1 is distinct from other known actin binding proteins in its effect on F-actin network structure. Recently, LSP1 was identified as the 47-kD protein overexpressed in the polymorphonuclear neutrophils of patients with a rare neutrophil disorder, neutrophil actin dysfunction with abnormalities of 47-kD and 89-kD proteins (NAD 47/89). Since its overexpression is implicated in the functional pathogenesis of a novel human neutrophil motile dysfunction and microfilamentous cytoskeletal abnormality (NAD 47/89), finding LSP1 in all human leukocytes suggests that it plays a role in regulating microfilamentous cytoskeleton structure and motile function in all leukocytes. The results show LSP1 is expressed in PMNs and suggest overexpression of LSP1 is related to the motility and cytoskeletal abnormalities in NAD 47/89 PMNs. These defects in NAD neutrophils are attributed to moderate over-expression of pp52 (LSP1), the F-actin-binding, leukocyte-specific phosphoprotein. Lymphocyte-specific protein 1 expression in eukaryotic cells reproduces the morphologic and motile abnormality of NAD 47/89 neutrophils. Human lymphocyte-specific protein 1, the protein overexpressed in neutrophil actin dysfunction with 47-kDa and 89-kDa protein abnormalities (NAD 47/89), has multiple F-actin binding domains. |
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